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Human IRAK4 Protein expressed in Baculovirus infected Insect Cells - ABIN2003326
Strelow, Kollewe, Wesche: Characterization of Pellino2, a substrate of IRAK1 and IRAK4. in FEBS letters 2003
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This is the first study to show an association between single nucleotide polymorphisms in IRAK1 (show IRAK1 Proteins), IRAK4 and MyD88 (show MYD88 Proteins), and the presence of severe invasive pneumococcal disease.
Src (show SRC Proteins), Syk (show SYK Proteins), IRAK1 (show IRAK1 Proteins), and IRAK4 have roles in anti-inflammatory responses mediated by dietary flavonoid Kaempferol
findings suggest that rare, functional variants in MYD88, IRAK4 or IKBKG do not significantly contribute to IPD susceptibility in adults at the population level
High mRNA levels of IRAK1 (show IRAK1 Proteins) and IRAK4 correlated with VKH disease activity.
Studies indicate that interleukin-1 receptor-associated kinase 4 protein (IRAK4), a serine/threonine kinase, plays a key role in both inflammation and oncology diseases.
by bolstering the IgM(+)IgD(+)CD27(+) B-cell subset, IRAK-4 and MyD88 promote optimal T-independent IgM antibody responses against bacteria in humans.
delineation of the latter responses identified a narrow repertoire of transcriptional programs affected by loss of MyD88 (show MYD88 Proteins) function or IRAK4 function
Data show that dimerization is crucial for IRAK4 autophosphorylation in vitro and ligand dependent signaling in cells.
these studies suggest that not only the loss of protein expression but also the defect of Myddosome formation couldcause IRAK4 and MyD88 (show MYD88 Proteins) deficiency syndromes.
IRAK4 is regulated by Interleukin 1/Toll (show TLR4 Proteins)-like receptor-induced autophosphorylation
PMA treatment during a vulnerable period can alter brain development. IL-18 and IRAK-4 appear to be important for the development of PMA induced injury.
enforced expression of miR (show MLXIP Proteins)-302b or IRAK4 siRNA silencing inhibits downstream NF-kappaB (show NFKB1 Proteins) signalling and airway leukocyte infiltration, thereby alleviating lung injury and increasing survival in P. aeruginosa-infected mice.
Our results demonstrate that osteoclasts and FBGCs are reciprocally regulated and identify IRAK4 as a potential therapeutic target to inhibit stimulated osteoclastogenesis and rescue inhibited FBGC formation
Suggest FC-99 is a potential therapeutic molecule that alleviated experimental sepsis by directly inhibiting IRAK4 activation.
MiR (show MLXIP Proteins)-93 inhibits IRAK4 expression by binding directly to the 3'-UTR of IRAK4.
Intact IRAK4 function inhibited heart-specific migration of bone-marrow-derived CCR5(+) cells.
In macrophages from IRAK4(KDKI) mice, IRAK4 kinase deficiency decreased LPS (show TLR4 Proteins) signaling but did not prevent endotoxin tolerance. A TLR2-TLR1 (show TLR1 Proteins) agonist attenuated TLR2-elicited homo- & heterotolerance at the level of MAPK (show MAPK1 Proteins) activation.
During bacterial infection, PGN (show SPG7 Proteins)-mediated TLR2 signaling induces miR (show MLXIP Proteins)-132/-212 to downregulate IRAK4.
IRAK4-deficient mice exhibit increased susceptibility and decreased cytokine production in vivo upon Streptococcus pneumoniae infection.
Experimental and natural infections in MyD88 (show MYD88 Proteins)- and IRAK-4-deficient mice and humans.
This gene encodes a kinase that activates NF-kappaB in both the Toll-like receptor (TLR) and T-cell receptor (TCR) signaling pathways. The protein is essential for most innate immune responses. Mutations in this gene result in IRAK4 deficiency and recurrent invasive pneumococcal disease. Multiple transcript variants encoding different isoforms have been found for this gene.
interleukin-1 receptor-associated kinase 4
, interleukin-1 receptor-associated kinase 4-like
, Interleukin-1 receptor-associated kinase 4
, renal carcinoma antigen NY-REN-64
, NY-REN-64 antigen
, interleukin-1 receptor associated kinase 4